Nakamura Y, Plumbridge J, Dondon J, Grunberg-Manago M
Gene. 1985;36(1-2):189-93. doi: 10.1016/0378-1119(85)90085-x.
Analysis of three different nusA mutant strains suggests that the expression of the nusA-infB operon of Escherichia coli is regulated autogenously by the nusA gene product, a protein known to mediate transcription termination and antitermination. The cellular amounts of NusA and IF2 (infB) proteins are enhanced by a nusAts mutation which causes reduced transcription-termination activity. A nusAam mutant carrying the am ts suppressor, supFts6, overproduces the IF2 protein when the amount of NusA protein is reduced by the thermal inactivation of the supFts6. A modified form of NusA with the cat protein of Mr of 24 000 attached to the C terminus of NusA is overproduced compared to the wild-type NusA and causes the overproduction of IF2.
对三种不同的nusA突变菌株的分析表明,大肠杆菌的nusA-infB操纵子的表达由nusA基因产物自主调节,nusA基因产物是一种已知介导转录终止和抗终止的蛋白质。nusAts突变会导致转录终止活性降低,从而增加NusA和IF2(infB)蛋白的细胞含量。携带am ts抑制子supFts6的nusAam突变体,当supFts6因热失活而使NusA蛋白量减少时,会过量产生IF2蛋白。与野生型NusA相比,一种在NusA的C末端连接了分子量为24000的cat蛋白的修饰形式的NusA过量产生,并导致IF2的过量产生。